2020
Lenárt, Sára; Lenárt, Peter; Šmarda, Jan; Remšík, Ján; Souček, Karel; Beneš, Petr
Trop2: Jack of All Trades, Master of None. Journal Article
In: Cancers, vol. 12, no. 11, 2020, ISSN: 2072-6694, (Place: Switzerland).
Abstract | Links | BibTeX | Tags: cancer, epithelial-to-mesenchymal transition, metastases, proliferation, TACSTD2, therapy, Trop2
@article{lenart_trop2_2020,
title = {Trop2: Jack of All Trades, Master of None.},
author = {Sára Lenárt and Peter Lenárt and Jan Šmarda and Ján Remšík and Karel Souček and Petr Beneš},
doi = {10.3390/cancers12113328},
issn = {2072-6694},
year = {2020},
date = {2020-11-01},
journal = {Cancers},
volume = {12},
number = {11},
abstract = {Trophoblast cell surface antigen 2 (Trop2) is a widely expressed glycoprotein and an epithelial cell adhesion molecule (EpCAM) family member. Although initially identified as a transmembrane protein, other subcellular localizations and processed forms were described. Its congenital mutations cause a gelatinous drop-like corneal dystrophy, a disease characterized by loss of barrier function in corneal epithelial cells. Trop2 is considered a stem cell marker and its expression associates with regenerative capacity in various tissues. Trop2 overexpression was described in tumors of different origins; however, functional studies revealed both oncogenic and tumor suppressor roles. Nevertheless, therapeutic potential of Trop2 was recognized and clinical studies with drug-antibody conjugates have been initiated in various cancer types. One of these agents, sacituzumab govitecan, has been recently granted an accelerated approval for therapy of metastatic triple-negative breast cancer. In this article, we review the current knowledge about the yet controversial function of Trop2 in homeostasis and pathology.},
note = {Place: Switzerland},
keywords = {cancer, epithelial-to-mesenchymal transition, metastases, proliferation, TACSTD2, therapy, Trop2},
pubstate = {published},
tppubtype = {article}
}
Trophoblast cell surface antigen 2 (Trop2) is a widely expressed glycoprotein and an epithelial cell adhesion molecule (EpCAM) family member. Although initially identified as a transmembrane protein, other subcellular localizations and processed forms were described. Its congenital mutations cause a gelatinous drop-like corneal dystrophy, a disease characterized by loss of barrier function in corneal epithelial cells. Trop2 is considered a stem cell marker and its expression associates with regenerative capacity in various tissues. Trop2 overexpression was described in tumors of different origins; however, functional studies revealed both oncogenic and tumor suppressor roles. Nevertheless, therapeutic potential of Trop2 was recognized and clinical studies with drug-antibody conjugates have been initiated in various cancer types. One of these agents, sacituzumab govitecan, has been recently granted an accelerated approval for therapy of metastatic triple-negative breast cancer. In this article, we review the current knowledge about the yet controversial function of Trop2 in homeostasis and pathology.